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Immunity

A-Level Biology 9700 · Topic 11 revision notes

Everything from the 4 lessons of this topic on a few pages: the key idea of each lesson, the diagram to remember, the points to learn and the traps examiners set. Read it, cover it, test yourself.

  1. Phagocytes and antigens
  2. Lymphocytes and the immune response
  3. Antibodies and monoclonal antibodies
  4. Vaccination and types of immunity

1Phagocytes and antigens

Syllabus 11.1

Phagocytes are white blood cells made in the bone marrow that engulf and digest pathogens. Neutrophils are short-lived, very numerous and the first to arrive at an infection; macrophages are larger, longer-lived cells that develop from monocytes in the tissues and, after digesting a pathogen, present its antigens to lymphocytes. Phagocytosis is non-specific: it is attracted by chemicals (chemotaxis), the pathogen is engulfed into a phagosome, lysosomes fuse with it and hydrolytic enzymes digest it. An antigen is a molecule, usually a protein or glycoprotein on a cell surface, that stimulates an immune response. Self antigens are the body's own and are tolerated; non-self antigens are foreign and trigger a response.

1 chemotaxis 2 engulfing 3 phagosome 4 digestion attracted tochemicals membrane flowsaround bacterium lysosomes fusewith the vacuole hydrolytic enzymesbreak it down bacterium lysosome phagocytosis by a neutrophil or macrophage: non-specific
Fig. 1: the four stages of phagocytosis

Non-specific first, specific later.

  • Chemotaxis, attach, engulf into a phagosome, lysosomes fuse, hydrolyse.
  • Neutrophils: many, short-lived, first to arrive.
  • Macrophages: long-lived, present antigens to lymphocytes.
  • Antigen = molecule that triggers a response; self tolerated, non-self attacked.

Watch out!

Phagocytosis is non-specific: the same neutrophil will engulf any pathogen it recognises as non-self. Do not say a phagocyte has receptors for one specific antigen; that is true of lymphocytes, not phagocytes.

An antigen is not a pathogen. A pathogen carries many different antigens, and a single antigen is the molecule that a lymphocyte receptor or an antibody binds to.

2Lymphocytes and the immune response

Syllabus 11.1

In a primary immune response a macrophage engulfs a pathogen and presents its antigens. The one T-helper cell with complementary receptors binds (clonal selection) and divides by mitosis (clonal expansion); its clones release cytokines. The B-lymphocyte with complementary receptors, stimulated by cytokines, divides into a clone that differentiates into plasma cells, which secrete specific antibodies, and memory cells. Cytokines also activate T-killer cells, which destroy infected body cells displaying the antigen. Because selection and cloning take days, the primary response is slow. Memory cells stay in the blood for years, so a second exposure to the same antigen triggers a secondary response that is faster and much larger: this is long-term immunity.

antibody concentration in the blood time → first exposure second exposure, same antigen primary slow, small secondary faster, larger, longer memory cells explain the difference
Fig. 1: antibody concentration in the primary and secondary immune responses

Every step has a named cell.

  • Macrophage presents; T-helper selected, cloned, releases cytokines.
  • B cell selected and cloned; becomes plasma cells + memory cells.
  • T-killer cells destroy infected body cells.
  • Secondary response: sooner, larger, longer, thanks to memory cells.

Watch out!

Clonal selection is not the lymphocyte "making" a receptor to fit the antigen. The lymphocyte with a complementary receptor already exists before the infection; the antigen only selects it.

Long-term immunity is due to memory cells, not to antibodies staying in the blood. Antibodies are broken down within weeks; memory cells remain.

3Antibodies and monoclonal antibodies

Syllabus 11.2

An antibody is a globular glycoprotein made by plasma cells. It has four polypeptide chains, two long heavy chains and two short light chains, held together by disulfide bonds. The tips form two variable regions whose antigen-binding sites are complementary to one specific antigen; the constant region is the same for a class of antibodies and binds to receptors on phagocytes; a hinge region gives flexibility. Antibodies cause agglutination, neutralise toxins and viruses and mark pathogens for phagocytosis (opsonisation). Monoclonal antibodies, identical antibodies from one clone, are made by the hybridoma method: B cells from an immunised mouse are fused with myeloma cells, and the hybridoma making the wanted antibody is selected and cloned. Because they bind one antigen, they are used to diagnose disease (pregnancy tests, locating cancers) and to treat it (targeting cancer cells).

antigen-binding site (variable region) antigen-binding site light chain heavy chain constant region (binds phagocyte receptors) disulfide bonds hinge region four polypeptide chains: quaternary structure
Fig. 1: the structure of an antibody molecule

Link every part to a job.

  • Variable region: antigen-binding site, complementary, two per antibody.
  • Constant region: binds phagocytes; hinge: flexibility; disulfide bonds: hold chains.
  • Hybridoma = B cell + myeloma: immunise, fuse, screen, clone.
  • Diagnosis: detect one antigen; treatment: target one cell type.

Watch out!

The antigen-binding site is in the variable region, made by both a heavy and a light chain. Do not put the binding site on the constant region, and do not call the variable region the "active site": that term is for enzymes.

A hybridoma is a fusion of a B-lymphocyte (or plasma cell) with a myeloma cell. Answers that fuse "a B cell with a T cell" or "two plasma cells" lose the mark.

4Vaccination and types of immunity

Syllabus 11.2

Active immunity develops when your own lymphocytes respond to an antigen, making plasma cells, antibodies and memory cells: it takes time but is long-lasting. Passive immunity is gained when antibodies made by another organism are received: it is immediate but short-lived, because the antibodies are broken down and no memory cells form. Immunity is natural when it comes from normal life (an infection, antibodies across the placenta or in breast milk) and artificial when it comes from medical intervention (a vaccine, an injection of antibodies). A vaccine contains antigens, as dead or weakened pathogens, toxoids, purified proteins or mRNA, that stimulate a primary response and memory cells without causing disease, giving long-term immunity. Vaccination programmes control the spread of disease because when a high proportion of people are immune, the pathogen rarely reaches a susceptible person: herd immunity protects even those who cannot be vaccinated.

natural artificial active passive own plasma+ memory cells antibodies given,no memory cells catching thedisease vaccination(antigens injectedor swallowed) antibodies across theplacenta or inbreast milk injection ofantibodies (forexample antitoxin) active: long-term, slow to start; passive: immediate but short-lived
Fig. 1: the four types of immunity

Who made the antibodies?

  • Active: you made them, memory cells, long-term.
  • Passive: given to you, no memory cells, short-term.
  • Natural = everyday life; artificial = medical intervention.
  • Vaccine = antigens; herd immunity = enough people immune to stop spread.

Watch out!

Passive immunity is short-lived because no memory cells are made, not because the antibodies are "weaker". Always mention memory cells when you compare active and passive immunity.

Herd immunity does not mean every person is immune. It means enough people are immune that the pathogen cannot keep spreading.

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